Strain Name:

FVB.129S4(B6)-Ptpn1tm1Bbk/Mmjax

Availability:

Cryopreserved - Ready for recovery     Available at the JAX MMRRC

Please refer to the Mutant Mouse Regional Resource Center (MMRRC) for information about FVB.129S4(B6)-Ptpn1tm1Bbk/Mmjax MMRRC Stock Number 032242.
These Ptpn1 (protein tyrosine phosphatase) knockout mice remain lean on a high fat diet, exhibit a decrease in adipocyte volume, increased glucose utilization and enhanced glucose tolerance. This mutant mouse strain may be useful in studies of energy regulation, diet-induced obesity and glucose metabolism.

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
GenerationN20pN1
Generation Definitions
 
Donating Investigator Benjamin Neel,   Ontario Cancer Institute

Description
Mice that are homozygous for the targeted mutation are viable and fertile. Homozygous males exhibit decreased body weight on a standard chow diet; weight gain in females is comparable to controls. On a 55% fat diet, both males and females remain lean. Although adipocyte cell number is not decreased, adipocyte volume is significantly decreased. Basal metabolic rate and total energy expenditure are increased in male homozygotes on high fat diet. Additionally, male homozygous mice exhibit decreased leptin levels, increased insulin sensitivity as a result of increased glucose utilization in skeletal muscle and enhanced glucose tolerance.

Heterozygous males exhibit decreased body weight on a standard chow diet; however, on a 55% fat diet weight gain is similar to wild-type. Leptin levels are decreased in heterozygous males on both chow and high-fat diets.

This mutant mouse strain may be useful in studies of energy regulation, diet-induced obesity and glucose metabolism.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
A targeting vector containing a neomycin resistance cassette was used to replace the ATG-coding region in exon 1 and 2.3 kb of flanking sequence. The construct was electroporated into 129S4/SvJae derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts. The resulting chimeric animals were crossed to C57BL/6J and then to FVB/NJ for 20 generations(see SNP note below). Upon arrival, mice were bred to FVB/NJ for at least 1 generation to establish the colony.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. One marker on Chromosome 7 is segregating.

Control Information

  Control
   001800 FVB/NJ
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Ptpn1tm1Bbk allele
012677   B6.129S4-Ptpn1tm1Bbk/Mmjax
View Strains carrying   Ptpn1tm1Bbk     (1 strain)

Strains carrying other alleles of Ptpn1
012679   B6;129S4-Ptpn1tm2Bbk/Mmjax
View Strains carrying other alleles of Ptpn1     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Diabetes Mellitus, Noninsulin-Dependent; NIDDM   (PTPN1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Ptpn1tm1Bbk/Ptpn1+

        involves: 129S4/SvJae * C57BL/6J
  • growth/size/body phenotype
  • abnormal postnatal growth/weight/body size
    • male heterozygotes weaned onto a chow diet gain less weight than wild-type males over a 15-week period   (MGI Ref ID J:63236)
    • in contrast, male heterozygotes fed a 55% fat diet gain similar amounts of weight as wild-type males   (MGI Ref ID J:63236)
    • no weight differences are noted in female heterozygotes fed a chow diet for 15 weeks post-weaning   (MGI Ref ID J:63236)
    • decreased body weight
      • on a high-fat diet, male heterozygotes weigh on average 10% less than wild-type males   (MGI Ref ID J:63236)
  • homeostasis/metabolism phenotype
  • decreased circulating insulin level
    • on a chow diet, serum insulin levels (fasted and fed) of male heterozygotes are similar to those of male homozygotes   (MGI Ref ID J:63236)
    • in contrast, on a high-fat diet, heterozygous serum insulin levels are comparable to those of wild-type mice, suggesting that (on this diet) one copy of the gene is sufficient to mediate its effects on energy expenditure and insulin action   (MGI Ref ID J:63236)
  • decreased circulating leptin level
    • on a chow diet, male heterozygotes show an ~60% reduction in fed serum leptin levels relative to wild-type males; a similar reduction is noted in male homozygotes   (MGI Ref ID J:63236)
    • on a high-fat diet, male heterozygotes show an intermediate reduction in fed serum leptin levels relative to wild-type and homozygous mutant males   (MGI Ref ID J:63236)

Ptpn1tm1Bbk/Ptpn1tm1Bbk

        involves: 129S4/SvJae * C57BL/6J
  • growth/size/body phenotype
  • abnormal body composition   (MGI Ref ID J:63236)
    • decreased body weight
      • by 15 weeks post-weaning, male homozygotes fed a chow diet weigh 16% less than wild-type males   (MGI Ref ID J:63236)
      • on a high fat diet, male homozygotes weigh on average 38% less than wild-type males   (MGI Ref ID J:63236)
      • reduced body weight is partly due to decreased lipid content in mutant adipocytes   (MGI Ref ID J:63236)
    • decreased percent body fat
      • on a high fat diet, male homozygotes show a significant reduction in the mass of white fat depots and body lipid content and a smaller reduction in fat-free dry mass   (MGI Ref ID J:63236)
      • notably, homozygotes display normal levels of serum free fatty acids in both the fed and fasted states relative to wild-type mice   (MGI Ref ID J:63236)
    • decreased percent water in carcass
      • on a high fat diet, male homozygotes show a decrease in total carcass water content relative to wild-type   (MGI Ref ID J:63236)
  • abnormal postnatal growth/weight/body size
    • male homozygotes weaned onto a chow diet gain less weight than wild-type males over a 15-week period; this difference becomes significant at 9 weeks post-weaning   (MGI Ref ID J:63236)
    • no weight differences are noted in female homozygotes fed a chow diet for 15 weeks post-weaning   (MGI Ref ID J:63236)
    • decreased body weight
      • by 15 weeks post-weaning, male homozygotes fed a chow diet weigh 16% less than wild-type males   (MGI Ref ID J:63236)
      • on a high fat diet, male homozygotes weigh on average 38% less than wild-type males   (MGI Ref ID J:63236)
      • reduced body weight is partly due to decreased lipid content in mutant adipocytes   (MGI Ref ID J:63236)
    • decreased susceptibility to diet-induced obesity
      • when fed a 55% fat (caloric content) diet for 4 months, male homozygotes remain lean, with peak weights comparable to those of mutant males on a chow diet   (MGI Ref ID J:63236)
      • female homozygotes fed the high-fat diet also display significantly lower weight gain relative to wild-type females   (MGI Ref ID J:63236)
  • homeostasis/metabolism phenotype
  • abnormal energy expenditure
    • on a high fat diet, male homozygotes dissipate excess energy as heat, rather than storing it as fat   (MGI Ref ID J:63236)
    • reduced metabolic efficiency results in resistance to diet-induced obesity   (MGI Ref ID J:63236)
    • decreased susceptibility to diet-induced obesity
      • when fed a 55% fat (caloric content) diet for 4 months, male homozygotes remain lean, with peak weights comparable to those of mutant males on a chow diet   (MGI Ref ID J:63236)
      • female homozygotes fed the high-fat diet also display significantly lower weight gain relative to wild-type females   (MGI Ref ID J:63236)
  • decreased circulating glucose level
    • on both a chow and a high-fat diet, male homozygotes display significantly reduced fasting and fed blood glucose levels relative to wild-type males   (MGI Ref ID J:63236)
  • decreased circulating insulin level
    • on a chow diet, serum insulin levels (fed but not fasted) of male homozygotes are significantly lower than those of wild-type males   (MGI Ref ID J:63236)
    • on a high-fat diet, serum insulin levels (both fed and fasted) of male homozygotes are significantly lower than those of wild-type males   (MGI Ref ID J:63236)
  • decreased circulating leptin level
    • on a chow diet, male homozygotes show a 64% reduction in serum leptin levels relative to wild-type males; notably, serum leptin levels remain low upon high-fat feeding   (MGI Ref ID J:63236)
  • improved glucose tolerance
    • chow-fed male homozygotes exhibit an enhanced ability to clear glucose from peripheral circulation during intraperitoneal glucose tolerance tests (GTTs)   (MGI Ref ID J:63236)
    • in contrast, blood glucose levels and GTTs remain unaltered in chow-fed mutant females   (MGI Ref ID J:63236)
  • increased basal metabolism
    • on a high fat diet, male homozygotes display a 22% increase in basal metabolic rate relative to wild-type males   (MGI Ref ID J:63236)
  • increased core body temperature
    • on a high fat diet, male homozygotes exhibit a significant increase in core body temperature relative to wild-type males   (MGI Ref ID J:63236)
  • increased insulin sensitivity
    • chow-fed male (but not female) homozygotes display enhanced insulin sensitivity in insulin tolerance tests; insulin sensitivity remains elevated on a high-fat diet   (MGI Ref ID J:63236)
    • homozygotes show enhanced insulin sensitivity in hyperinsulinemic-euglycemic clamp studies, as shown by notable increases in rates of whole-body glucose disposal, glycolysis, and nonoxidative glucose metabolism   (MGI Ref ID J:63236)
    • interestingly, insulin sensitivity increases specifically in skeletal muscle, not in white adipose tissue   (MGI Ref ID J:63236)
  • adipose tissue phenotype
  • abnormal fat cell morphology
    • male homozygotes show a 2.6-fold decrease in average adipocyte volume; in contrast, adipocyte cell number remains unaffected   (MGI Ref ID J:63236)
  • abnormal fat pad morphology
    • on a 55% fat diet, male homozygotes show a 3-fold reduction in subcutaneous fat pad weights relative to wild-type males   (MGI Ref ID J:63236)
    • decreased epididymal fat pad weight
      • on a 55% fat diet, male homozygotes show a 3-fold reduction in epididymal fat pad weights relative to wild-type males   (MGI Ref ID J:63236)
    • decreased inguinal fat pad weight
      • on a 55% fat diet, male homozygotes show a 3-fold reduction in inguinal fat pad weights relative to wild-type males   (MGI Ref ID J:63236)
    • decreased interscapular fat pad weight
      • on a 55% fat diet, male homozygotes show a 3-fold reduction in interscapular fat pad weights relative to wild-type males   (MGI Ref ID J:63236)
  • decreased percent body fat
    • on a high fat diet, male homozygotes show a significant reduction in the mass of white fat depots and body lipid content and a smaller reduction in fat-free dry mass   (MGI Ref ID J:63236)
    • notably, homozygotes display normal levels of serum free fatty acids in both the fed and fasted states relative to wild-type mice   (MGI Ref ID J:63236)
  • decreased white adipose tissue amount
    • on a chow diet, male homozygotes show a 3-fold reduction in white fat pad mass relative to wild-type mice; brown adipose tissue mass remains unaffected   (MGI Ref ID J:63236)
  • behavior/neurological phenotype
  • abnormal food intake
    • male homozygotes tend to display a higher food intake than wild-type mice, but show normal stool mass with no detectable lipids   (MGI Ref ID J:63236)
  • endocrine/exocrine gland phenotype
  • *normal* endocrine/exocrine gland phenotype
    • on a high fat diet, male homozygotes display normal serum thyroxine (T4) levels relative to wild-type males   (MGI Ref ID J:63236)

Ptpn1tm1Bbk/Ptpn1tm1Bbk

        involves: 129/Sv * C57BL/6
  • endocrine/exocrine gland phenotype
  • abnormal pancreatic beta cell morphology
    • homozygotes display a reduction in pancreatic cross-sectional beta-cell area relative to wild-type mice   (MGI Ref ID J:87249)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Diabetes and Obesity Research
Obesity Without Diabetes
      diet-induced, resistant

Metabolism Research

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ptpn1tm1Bbk
Allele Name targeted mutation 1, Barabra B Kahn
Allele Type Targeted (Null/Knockout)
Common Name(s) Ex1-; PTP-1B-; PTP1B-;
Mutation Made By Benjamin Neel,   Ontario Cancer Institute
Strain of Origin129S4/SvJae
Gene Symbol and Name Ptpn1, protein tyrosine phosphatase, non-receptor type 1
Chromosome 2
Gene Common Name(s) PTP-1B; PTP1B; Ptp;
Molecular Note Exon 1 and surrounding sequence were replaced with a neomycin selection cassette. The absence of transcript and protein in homozygous mutant mice was verified by Northern and Western blot analyses of a variety of tissues. [MGI Ref ID J:63236]

Genotyping

Genotyping Information

Genotyping Protocols

Ptpn1tm1Bbk, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Klaman LD; Boss O; Peroni OD; Kim JK; Martino JL; Zabolotny JM; Moghal N; Lubkin M; Kim YB; Sharpe AH; Stricker-Krongrad A; Shulman GI; Neel BG; Kahn BB. 2000. Increased energy expenditure, decreased adiposity, and tissue-specific insulin sensitivity in protein-tyrosine phosphatase 1B-deficient mice. Mol Cell Biol 20(15):5479-89. [PubMed: 10891488]  [MGI Ref ID J:63236]

Additional References

Ptpn1tm1Bbk related

Agouni A; Mody N; Owen C; Czopek A; Zimmer D; Bentires-Alj M; Bence KK; Delibegovic M. 2011. Liver-specific deletion of protein tyrosine phosphatase (PTP) 1B improves obesity- and pharmacologically induced endoplasmic reticulum stress. Biochem J 438(2):369-78. [PubMed: 21605081]  [MGI Ref ID J:177894]

Arroba AI; Revuelta-Cervantes J; Menes L; Gonzalez-Rodriguez A; Pardo V; de la Villa P; Burks DJ; Valverde AM. 2013. Loss of protein tyrosine phosphatase 1B increases IGF-I receptor tyrosine phosphorylation but does not rescue retinal defects in IRS2-deficient mice. Invest Ophthalmol Vis Sci 54(6):4215-25. [PubMed: 23702782]  [MGI Ref ID J:214039]

Bence KK; Delibegovic M; Xue B; Gorgun CZ; Hotamisligil GS; Neel BG; Kahn BB. 2006. Neuronal PTP1B regulates body weight, adiposity and leptin action. Nat Med 12(8):917-24. [PubMed: 16845389]  [MGI Ref ID J:111969]

Bentires-Alj M; Neel BG. 2007. Protein-tyrosine phosphatase 1B is required for HER2/Neu-induced breast cancer. Cancer Res 67(6):2420-4. [PubMed: 17347513]  [MGI Ref ID J:120339]

Fernandez-Ruiz R; Vieira E; Garcia-Roves PM; Gomis R. 2014. Protein tyrosine phosphatase-1B modulates pancreatic beta-cell mass. PLoS One 9(2):e90344. [PubMed: 24587334]  [MGI Ref ID J:214467]

Gonzalez-Rodriguez A; Clampit JE; Escribano O; Benito M; Rondinone CM; Valverde AM. 2007. Developmental switch from prolonged insulin action to increased insulin sensitivity in protein tyrosine phosphatase 1B-deficient hepatocytes. Endocrinology 148(2):594-608. [PubMed: 17068137]  [MGI Ref ID J:129555]

Gonzalez-Rodriguez A; Mas Gutierrez JA; Sanz-Gonzalez S; Ros M; Burks DJ; Valverde AM. 2010. Inhibition of PTP1B restores IRS1-mediated hepatic insulin signaling in IRS2-deficient mice. Diabetes 59(3):588-99. [PubMed: 20028942]  [MGI Ref ID J:164152]

Julien SG; Dube N; Read M; Penney J; Paquet M; Han Y; Kennedy BP; Muller WJ; Tremblay ML. 2007. Protein tyrosine phosphatase 1B deficiency or inhibition delays ErbB2-induced mammary tumorigenesis and protects from lung metastasis. Nat Genet 39(3):338-46. [PubMed: 17259984]  [MGI Ref ID J:120342]

Kant S; Swat W; Zhang S; Zhang ZY; Neel BG; Flavell RA; Davis RJ. 2011. TNF-stimulated MAP kinase activation mediated by a Rho family GTPase signaling pathway. Genes Dev 25(19):2069-78. [PubMed: 21979919]  [MGI Ref ID J:177426]

Kim IS; Baek SH. 2010. Mouse models for breast cancer metastasis. Biochem Biophys Res Commun 394(3):443-7. [PubMed: 20230796]  [MGI Ref ID J:159230]

Kushner JA; Haj FG; Klaman LD; Dow MA; Kahn BB; Neel BG; White MF. 2004. Islet-Sparing Effects of Protein Tyrosine Phosphatase-1b Deficiency Delays Onset of Diabetes in IRS2 Knockout Mice. Diabetes 53(1):61-66. [PubMed: 14693698]  [MGI Ref ID J:87249]

Lee MN; Roy M; Ong SE; Mertins P; Villani AC; Li W; Dotiwala F; Sen J; Doench JG; Orzalli MH; Kramnik I; Knipe DM; Lieberman J; Carr SA; Hacohen N. 2012. Identification of regulators of the innate immune response to cytosolic DNA and retroviral infection by an integrative approach. Nat Immunol 14(2):179-85. [PubMed: 23263557]  [MGI Ref ID J:192611]

Milani ES; Brinkhaus H; Dueggeli R; Klebba I; Mueller U; Stadler M; Kohler H; Smalley MJ; Bentires-Alj M. 2013. Protein tyrosine phosphatase 1B restrains mammary alveologenesis and secretory differentiation. Development 140(1):117-25. [PubMed: 23154416]  [MGI Ref ID J:191078]

Nieto-Vazquez I; Fernandez-Veledo S; de Alvaro C; Rondinone CM; Valverde AM; Lorenzo M. 2007. Protein-tyrosine phosphatase 1B-deficient myocytes show increased insulin sensitivity and protection against tumor necrosis factor-alpha-induced insulin resistance. Diabetes 56(2):404-13. [PubMed: 17259385]  [MGI Ref ID J:121942]

Rajala RV; Tanito M; Neel BG; Rajala A. 2010. Enhanced retinal insulin receptor-activated neuroprotective survival signal in mice lacking the protein-tyrosine phosphatase-1B gene. J Biol Chem 285(12):8894-904. [PubMed: 20061388]  [MGI Ref ID J:161083]

Revuelta-Cervantes J; Mayoral R; Miranda S; Gonzalez-Rodriguez A; Fernandez M; Martin-Sanz P; Valverde AM. 2011. Protein Tyrosine Phosphatase 1B (PTP1B) Deficiency Accelerates Hepatic Regeneration in Mice. Am J Pathol 178(4):1591-604. [PubMed: 21406170]  [MGI Ref ID J:169922]

Xue B; Kim YB; Lee A; Toschi E; Bonner-Weir S; Kahn CR; Neel BG; Kahn BB. 2007. Protein-tyrosine phosphatase 1B deficiency reduces insulin resistance and the diabetic phenotype in mice with polygenic insulin resistance. J Biol Chem 282(33):23829-40. [PubMed: 17545163]  [MGI Ref ID J:124807]

Xue B; Pulinilkunnil T; Murano I; Bence KK; He H; Minokoshi Y; Asakura K; Lee A; Haj F; Furukawa N; Catalano KJ; Delibegovic M; Balschi JA; Cinti S; Neel BG; Kahn BB. 2009. Neuronal protein tyrosine phosphatase 1B deficiency results in inhibition of hypothalamic AMPK and isoform-specific activation of AMPK in peripheral tissues. Mol Cell Biol 29(16):4563-73. [PubMed: 19528236]  [MGI Ref ID J:151519]

Zhang J; Wang B; Zhang W; Wei Y; Bian Z; Zhang CY; Li L; Zen K. 2013. Protein tyrosine phosphatase 1B deficiency ameliorates murine experimental colitis via the expansion of myeloid-derived suppressor cells. PLoS One 8(8):e70828. [PubMed: 23951017]  [MGI Ref ID J:204928]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryWhile maintaining a live colony, these mice are bred as homozygotes.

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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